Potential Nutraceutical Properties of Leaves from Several Commonly Cultivated Plants.

Hafsa Amat-Ur-Rasool,David Tooth,Fenella Symes,Mehboob Ahmed,Shahida Hasnain,Larissa-Nele Schaffert,Wayne G Carter,Ekramy Elmorsy

doi:10.3390/biom10111556

Abstract

Chronic dietary ingestion of suitable phytochemicals may assist with limiting or negating neurodegenerative decline. Current therapeutics used to treat Alzheimer disease elicit broad adverse drug reactions, and alternative sources of cholinesterase inhibitors (ChEIs) are required. Herein, we screened methanolic extracts from seven commonly cultivated plants for their nutraceutical potential; ability to inhibit acetylcholinesterase (AChE) and butyryl-cholinesterase (BuChE), and provision of antioxidant activity through their 2,2-diphenyl-1-picryl-hydrazyl-hydrate (DPPH) free radical scavenging capabilities. Potential neurotoxicity of plant extracts was examined via application to SHSY-5Y neuroblastoma cells and quantitation of cell viability. Methanolic extracts of Citrus limon (Lemon), Bombax ceiba (Red silk-cotton), Lawsonia inermis (Henna), Eucalyptus globulus (Eucalyptus), Ocimum basilicum (Basil), Citrus reticulata (Mandarin orange), and Mentha spicata (Spearmint) all displayed concentration-dependent inhibition of AChE and BuChE. The majority of extracts inhibited AChE and BuChE to near equipotency, with Henna and Eucalyptus extracts the two most potent ChEIs. All plant extracts were able to scavenge free radicals in a concentration-dependent manner, with Eucalyptus the most potent antioxidant. Toxicity of plant extracts to neuronal cells was concentration dependent, with Eucalyptus also the most toxic extract. Fractionation of plant extracts and analysis by mass spectrometry identified a number of plant polyphenols that might have contributed to the cholinesterase inhibition: 3-caffeoylquinic acid, methyl 4-caffeoylquinate, kaempferol-acetyl-glycoside, quercetin 3-rutinoside, quercetin-acetyl-glycoside, kaempferol 3-O-glucoside, and quercetin 3-O-glucoside. In silico molecular modeling of these polyphenols demonstrated their improved AChE and BuChE binding affinities compared to the current FDA-approved dual ChEI, galantamine. Collectively, all the plant extracts contained nutraceutical agents as antioxidants and ChEIs and, therefore, their chronic consumption may prove beneficial to combat the pathological deficits that accrue in Alzheimer disease.

Highlights

We are living longer and with a demographic shift such that the proportion of the population over 60 has grown dramatically, estimated to be approximately 1 billion in 2017 but expected to double by 2050 [1]
We investigated the nutraceutical potential of leaves from seven commonly cultivated plants: Lemon (Citrus limon), Red silk-cotton (Bombax ceiba), Henna (Lawsonia inermis), Eucalyptus (Eucalyptus globulus), Basil (Ocimum basilicum), Mandarin Orange (Citrus reticulata), and Spearmint (Mentha spicata)
Patients suffering from Alzheimer disease (AD) represent the greatest number of dementia cases, and deployment of cholinesterase inhibitors (ChEIs) are the first-line drugs to abate the cholinergic deficit that contributes to impaired cognition [45]

Summary

Introduction

We are living longer and with a demographic shift such that the proportion of the population over 60 has grown dramatically, estimated to be approximately 1 billion in 2017 but expected to double by 2050 [1]. As a consequence of population growth, the number of people living with dementia doubled between 1990 and 2016 to approximately 44 million [2] and the current number of approximately 50 million sufferers is expected to triple by 2050 [3]. The benefits of diets rich in fruits and vegetables as well as a low consumption of alcohol have been purported to contribute to reduced dementia risk and the health and longevity associated with a ‘Mediterranean lifestyle’ [9,10,11,12,13,14]. One of the proposed mechanisms responsible for the health benefits of certain foods and supplements is the provision of natural antioxidants that may balance age-related oxidative damage and limit the pathological changes associated with neurodegeneration [15,16,17]

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Conclusion